Comparison of CLL and MCL primary cells obtained from a patient with MCL variant Richter syndrome
Mantle cell lymphoma-variant Richter syndrome: Detailed molecular-cytogenetic and backtracking analysis reveals slow evolution of a pre-MCL clone in parallel with CLL over several years.
Specimen part, Disease, Disease stage
View SamplesThe Drosophila insulator-binding proteins (IBPs) dCTCF/Beaf32 mark the physical borders of chromosomal domains involving co-factors that participate in long-range interactions. Chromosomal borders are further enriched in specific histone modifications yet the implication of histone modifiers and nucleosome dynamics remains largely unknown in such context. Here, we show that IBP depletion impairs nucleosome dynamics over genes flanked by their binding sites. Biochemical purification identifies a key histone methyltransferase of H3K36, NSD/dMes-4, as a novel co-factor of IBPs involved in chromatin accessibility, which specifically co-regulates hundreds of genes flanked by Beaf32/dCTCF. dMes-4 presets chromatin before the recruitment of transcriptional activators including DREF that triggers Set2/Hypb-mediated H3K36me3, RNA splicing and nucleosome positioning. Our results unveil a model for how IBPs regulate gene expression and nucleosome dynamics through NSD/dMes-4, which may contribute to regulate H3K27me3 spreading. Together, our data suggest a division of labor for how IBPs may dynamically regulate chromatin organization depending on distinct co-factors. Overall design: mRNA profiles of Beaf32-depleted or Wild-Type control Drosophila S2 cells by RNASeq (Illumina)
Insulators recruit histone methyltransferase dMes4 to regulate chromatin of flanking genes.
Cell line, Subject
View SamplesWe performed RNA-sequencing in c-Kit+ cells that were infected with retroviruses expressing shRNAs for Renilla, Rad21, Smc1a, Smc3 or Stag2. These cells were grown in methylcellulose (M3434) for either one passage (P1) or replated for five passages (P5). Overall design: RNA-sequencing control (Ren) and cohesin (Rad21, Smc1a, Smc3 and Stag2) knockdown cells.
Cohesin loss alters adult hematopoietic stem cell homeostasis, leading to myeloproliferative neoplasms.
Specimen part, Subject
View SamplesWe performed RNA-sequencing in LSK cells (Lin(neg)/c-Kit(+)/Sca-1(+)) from shRNA mice carrying an shRNA for Renilla, Smc1a or Stag2. Overall design: RNA-sequencing control (Renilla) and cohesin (Smc1a and Stag2) knockdown cells.
Cohesin loss alters adult hematopoietic stem cell homeostasis, leading to myeloproliferative neoplasms.
Specimen part, Subject
View SamplesWe investigate the contribution of IRE1 signaling to the modulation of U87 glioma cells transcriptome upon various stresses. To this end, IRE1 control and IRE1 dominant negative expressing U87 glioma cells were subjected to environmental or chemical challenges and their transcriptome monitored using Affymetrix microarrays.
Posttranscriptional regulation of PER1 underlies the oncogenic function of IREα.
Cell line, Treatment
View SamplesGlioblastoma multiforme is the most lethal form of glioma with an overall survival at 5 years nearly null, which mainly results from acquired resistance to therapies. Large scale sequencing studies on human cancer biopsies defined IRE1alpha as the fifth most oncogenic mutated kinase in human cancer. IRE1alpha is a major component of the Unfolded Protein Response signaling and increasing evidence suggests that it is a central player in GBM development.
Dual IRE1 RNase functions dictate glioblastoma development.
Specimen part, Cell line
View Samples